[Discussion between informal and formal caregivers of community-dwelling older adults]. / Overleg tussen mantelzorgers en formele hulpverleners van thuiswonende ouderen.

Current Dutch policy on long-term care is aimed at a stronger connection between formal home care and informal care. We examined if formal and informal caregivers of community-dwelling older adults discuss the care and whether this is related to characteristics of the older adult, the care network and the individual caregivers. Data are derived from 63 community-dwelling older adults, including their health, their perceived control of the care and their care network. In addition, 79 informal and 90 formal caregivers are interviewed on their motives and vision on caregiving. The 112 dyads between those formal and informal caregivers are the units of analysis in the current study. Bivariate analyses reveal that informal caregivers are more likely to discuss the care with formal caregivers when they are residing with the older adult, when they provide a lot of care and/or when they are strongly motivated to keep the older adult at home. This is particularly the case when the care demands are high. Characteristics of the formal caregivers were not important. In conclusion, discussion of care between non-resident informal caregivers and formal caregivers is not self-evident and requires more effort to be established.

Cardiopulmonary bypass and circulatory arrest increase endothelin-1 production and receptor expression in the lung.

BACKGROUND: Endothelin-1 has been shown to be a mediator of pulmonary hypertension after cardiopulmonary bypass and deep hypothermic circulatory arrest. It is not known whether the mechanism is increased production of endothelin-1 or alterations in expression of endothelin-1 receptors in the lung. This study was designed to test the hypothesis that circulatory arrest increases endothelin-1 mRNA levels and endothelin-1 receptor expression in the lung. METHODS AND RESULTS: Twenty-four piglets (7 to 30 days old) were studied randomly either at baseline (controls, n = 12) or after cardiopulmonary bypass with 30 minutes of circulatory arrest (deep hypothermic circulatory arrest, n = 12). Lungs and pulmonary arteries were harvested immediately after hemodynamic data collection. Deep hypothermic circulatory arrest significantly increased pulmonary vascular resistance (p < 0.01). Deep hypothermic circulatory arrest also produced a significant increase in endothelin-1 mRNA levels in the pulmonary arteries (149 +/- 55 pg vs 547 +/- 111 pg, p = 0.007). There was no significant change in the pulmonary parenchymal endothelin-1 mRNA levels (4102 +/- 379 pg vs 4623 +/- 308 pg, p = 0.32). Ligand binding studies of the lung parenchyma revealed a single specific endothelin-1 binding site with an EC50 value (effective concentration causing 50% of the maximum response) of about 1 x 10(-8) mol/L, consistent with the endothelin B subtype. Deep hypothermic circulatory arrest resulted in a significant increase in the number of endothelin-1 receptors in the lung (109 +/- 6 fmol/mg total protein to 135 +/- 9 fmol/mg total protein, p = 0.02). CONCLUSIONS: Deep hypothermic circulatory arrest increases production of endothelin-1 by the pulmonary vascular endothelium. Endothelin-1 production in the pulmonary parenchyma does not change. Expression of endothelin B receptors in the pulmonary parenchyma also increases after cardiopulmonary bypass with deep hypothermic circulatory arrest. This study supports the hypothesis that deep hypothermic circulatory arrest results in pulmonary vascular endothelial activation with increased endothelin-1 mRNA production.

Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung.

Endothelial injury with failure of pulmonary endothelium-dependent vasodilatation has been proposed as a possible cause for the increased pulmonary vascular resistance observed after cardiopulmonary bypass, but the mechanisms underlying this response are not understood. An in vivo piglet model was used to investigate the role of endothelium-dependent vasodilatation in postbypass pulmonary hypertension. The pulmonary vascular responses to acetylcholine, a receptor-mediated endothelium-dependent vasodilator, and nitric oxide, an endothelium-independent vasodilator, were studied in one group of animals after preconstriction with the thromboxane A2 analog U46619 (n = 6); a second group was studied after bypass with 30 minutes of deep hypothermic circulatory arrest (n = 6). After preconstriction with U46619, both acetylcholine and nitric oxide caused significant decreases in pulmonary vascular resistance (34% +/- 6% decrease, p = 0.007, and 39% +/- 4% decrease, p = 0.001). After cardiopulmonary bypass with circulatory arrest, acetylcholine did not significantly change pulmonary vascular resistance (0% +/- 8% decrease, p = 1.0), whereas nitric oxide produced a 32% +/- 4% decrease in pulmonary vascular resistance (p = 0.007). These results demonstrate a loss of receptor-mediated endothelium-dependent vasodilatation with normal vascular smooth muscle function after circulatory arrest. Administration of the nitric oxide synthase blocker Ngamma-nitro-L-arginine-methyl-ester after circulatory arrest significantly increased pulmonary vascular resistance; thus, although endothelial cell production of nitric oxide may be diminished, it continues to be a major contributor to pulmonary vasomotor tone after cardiopulmonary bypass with deep hypothermic circulatory arrest. In summary, cardiopulmonary bypass with deep hypothermic circulatory arrest results in selective pulmonary endothelial cell dysfunction with loss of receptor-mediated endothelium-dependent vasodilatation despite preserved ability of the endothelium to produce nitric oxide and intact vascular smooth muscle function.

Nitric oxide production affects cerebral perfusion and metabolism after deep hypothermic circulatory arrest.

BACKGROUND: Use of deep hypothermic circulatory arrest (DHCA) in infant cardiac surgery is associated with reduced cerebral perfusion and metabolism during the recovery period. We investigated the impairment of nitric oxide production as a possible cause. METHODS: A group of 1-week-old piglets underwent normothermic cardiopulmonary bypass (group A); three other groups (B, C, and D; n = 6 per group) underwent 60 minutes of DHCA at 18 degrees C and 60 minutes of rewarming. The animals were then treated as follows: Groups A and B received L-omega-nitro-arginine-methyl-ester (L-NAME, 50 mg.kg-1); group C, saline solution; and group D, L-arginine (600 mg.kg-1). RESULTS: In group A, global cerebral blood flow decreased to 37.3% +/- 4.2% of baseline after L-NAME administration (p < 0.005). In group B, global cerebral blood flow decreased to 44.6% +/- 4.4% of baseline after DHCA and 28.9% +/- 3.4% after L-NAME administration (p < 0.001). Following L-arginine treatment after DHCA (group D), global cerebral blood flow increased from 43.8% +/- 3.0% of baseline to 61.6% +/- 9.1% (p < 0.05); cerebral oxygen metabolism increased from 1.93 +/- 0.16 mL.min-1.100 g-1 after DHCA to 2.42 +/- 0.25 mL.min-1.100 g-1 (p < 0.05). CONCLUSIONS: Tonal production of nitric oxide is impaired in the brain after DHCA and is partly responsible for the circulatory and metabolic changes observed. Stimulation of nitric oxide production (L-arginine) significantly improved recovery of cerebral blood flow and cerebral oxygen metabolism after DHCA.

Thromboxane A2-receptor blockade improves cerebral protection for deep hypothermic circulatory arrest.

OBJECTIVE: Following the use of deep hypothermic circulatory arrest in cardiac surgery, cerebral blood flow and cerebral oxygen metabolism are impaired. These may result from abnormal cerebral vasospasm. Powerful vasoconstrictors including endothelins and thromboxane A2 could mediate these processes. We investigated possible involvement of these two factors by assessing the effects of (a) phosphoramidon-an inhibitor of endothelin converting enzyme, and (b) vapiprost (GR32191B)-a specific thromboxane A2-receptor antagonist, on the recovery of cerebral blood flow and cerebral oxygen metabolism following deep hypothermic circulatory arrest. METHODS: A total of 18 1-week-old piglets were randomised into three groups (n = 6 per group). At induction, the control group received saline; group PHOS received phosphoramidon 30 mg kg-1 intravenously. Group VAP received vapiprost 2 mg kg-1 at induction and at 30 min intervals thereafter. All groups underwent cardiopulmonary bypass cooling to 18 degrees C, exposed to 60 min of deep hypothermic circulatory arrest, rewarmed and reperfused for 1 h. Cerebral blood flow was measured with radio-labeled microspheres: cerebral oxygen metabolism was calculated at baseline before deep hypothermic circulatory arrest and at 1 h of reperfusion and rewarming. RESULTS: In the control group, cerebral blood flow decreased to 40.2 +/- 2.0% of baseline after deep hypothermic circulatory arrest and cerebral oxygen metabolism decreased to 50.0 +/- 5.5% (P < 0.0005). The responses in group PHOS were similar. In group VAP, cerebral blood flow and cerebral oxygen metabolism were 64.3 +/- 10.6 and 80.1 +/- 9.8% of baseline, respectively, after deep hypothermic circulatory arrest. Thus, treatment with vapiprost significantly improved recovery of cerebral blood flow (P = 0.046) and cerebral oxygen metabolism (P = 0.020) following deep hypothermic circulatory arrest. No such improvement was seen after treatment with phosphoramidon. CONCLUSIONS: Thromboxane A2 mediates impairments in cerebral perfusion and metabolism following deep hypothermic circulatory arrest. These changes were attenuated by blockade of thromboxane A2-receptors using vapiprost. Endothelins are not shown to be involved. Better knowledge of injury mechanisms will enable development of more effective cerebral protection strategies and allow safer application of deep hypothermic circulatory arrest.